Feline leukemia virus (FeLV), is an etiological agent for generalized immunosuppression in the infected cats. Cats with FeLV-induced immunosuppression have immune deficiencies and dysfunctions which resemble acquired immune deficiency syndrome (AIDS). Recent studies suggest a human type C retrovirus as a possible etiological agent for AIDS. It is therefore important to understand the mechanism(s) of retrovirus-induced immunosuppression and immunological diseases. FeLV-infected cats have defects in T-cell functions, such as suppressed blastogenic responses to T-cell mitogens and impaired production of a T-cell lymphokine, gamma-interferon (IFN-gamma). It is possible that these defects in the host immune system could play a role in the pathogenesis of the immunosuppression, as well as in the leukemias and lymphomas caused by this virus. Lymphokines such as interleukin-2 (IL-2) and interferons (IFN-gamma and IFN-alpha) regulate host immune system. Consequently, any defects in the production or function of these lymphokines could contribute to the pathogenesis of the FeLV-induced immunosuppression and diseases. Therefore, studies will be performed on FeLV-infected cats to determine the role of feline lymphokines, IL-2 and IFNs, in FeLV-induced immunosuppression, leukemias, and lymphomas. FeLV and a FeLV protein, p15E, suppress mitogen-induced blastogenesis of normal cat lymphocytes. However, nothing is known about the direct effects of FeLV and FeLV proteins on lymphokine productions. This study will investigate the direct effects of FeLV and FeLV proteins on lymphokine productions and activities and those of purified lymphokines on FeLV infectivity and FeLV-induced immunosuppression, leukemia, and lymphoma. IFN therapy will be conducted on FeLV-infected cats with leukemias and lymphomas. (IS)